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1.
J Viral Hepat ; 28(1): 61-71, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-32896077

RESUMO

Previous observational studies suggested that hepatitis B virus (HBV) preS mutation plays an important role in the existence of HBV-related hepatocellular carcinoma (HCC). However, the results are still debatable. With an increasing number of studies about this topic, this study employed a meta-analysis to identify the association between HBV preS mutation and HCC risk. We searched for eligible studies from PubMed, ProQuest, CINAHL, ScienceDirect and Springer databases to assess the association between HBV mutation and HCC risk. This meta-analysis was conducted using RevMan 5.3 to provide pooled estimate for odds ratio (ORs) with 95% confidence intervals (95% CIs). Twenty-one clinical studies were included in this meta-analysis study which consisted of 1738 participants with HBV-related HCC and 3740 HBsAg-positive patients without HCC. All studies used samples of Asian population. PreS deletion was the most common mutation found in all studies. We found that ORs of HBV overall preS deletion was associated with HCC (OR = 3.28; 95% CI = 2.32-4.65; P < .00001; random-effects model). Each preS1 and preS2 deletion was associated with increased risk of HCC, with OR 2.42 (95% CI = 1.25-4.68, P = .008) and 3.36 (95% CI = 2.04-5.55, P < .00001), respectively. PreS2 start codon mutation was also significantly associated with HCC risk (OR = 2.47; 95% CI: 1.15-5.27; P = .02; random-effect model). The result of this meta-analysis suggested that HBV preS deletion (all, preS1 and preS2) and preS2 start codon mutation might contribute to the increased risk of HBV-related HCC.


Assuntos
Carcinoma Hepatocelular , Antígenos de Superfície da Hepatite B/genética , Hepatite B Crônica , Hepatite B , Neoplasias Hepáticas , Precursores de Proteínas/genética , Carcinoma Hepatocelular/epidemiologia , Hepatite B/complicações , Vírus da Hepatite B/genética , Hepatite B Crônica/complicações , Humanos , Neoplasias Hepáticas/epidemiologia , Mutação
2.
BMC Cancer ; 20(1): 1134, 2020 Nov 23.
Artigo em Inglês | MEDLINE | ID: mdl-33228594

RESUMO

BACKGROUND: Research focusing on the relationship between five types of tumor necrosis factor-alpha (TNF-α) SNPs and the risk of hepatocellular carcinoma (HCC) were still controversial. Hereby, we performed a meta-analysis to determine the association between TNF-α promoter SNPs: -1031 T/C, - 863 C/A, - 857 C/T, - 308 G/A, and - 238 G/A with HCC risk. METHODS: We interrogated articles from journal database: PubMed, Pro-Quest, EBSCO, Science Direct, and Springer to determine the relationship between five types of SNPs in TNF-α gene with HCC risk. RevMan 5.3 software was used for analysis in fixed/random effect models. RESULTS: This meta-analysis included 23 potential articles from 2004 to 2018 with 3237 HCC cases and 4843 controls. We found that SNP - 863 C/A were associated with a significantly increased HCC risk (A vs C, OR = 1.31, 95% CI = 1.03-1.67). Similar results were obtained in - 857 C/T (TT/CT vs CC, OR = 1.31, 95% CI = 1.06-1.62), - 308 G/A (AA vs GG, OR = 3.14, 95% CI = 2.06-4.79), and - 238 G/A (AA vs GG, OR = 3.87, 95% CI = 1.32-11.34). While no associations were observed between SNP TNF-α - 1031 T/C and HCC risk. CONCLUSIONS: The present meta-analysis showed that TNFα SNPs -863C/A, - 857 C/T, - 308 G/A, and - 238 G/A were associated with the risk of HCC.


Assuntos
Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , Polimorfismo Genético/genética , Polimorfismo de Nucleotídeo Único/genética , Fator de Necrose Tumoral alfa/genética , Carcinoma Hepatocelular/patologia , Humanos , Neoplasias Hepáticas/patologia , Fatores de Risco
3.
ARYA Atheroscler ; 19(2): 8-13, 2023 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38883573

RESUMO

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Acute coronary syndrome is a manifestation of CVD. In Indonesia, limited studies have been conducted on genetics as a potential risk factor for acute coronary syndrome (ACS). Consequently, this study aimed to examine the effect of the methylenetetrahydrofolate reductase (MTHFR) A1298C gene polymorphism on the incidence of ACS. METHOD: The study employed a case-control design. Outpatients from the cardiology and internal medicine clinics at the University of Airlangga (UNAIR) Hospital in Surabaya, Indonesia, constituted the study population. The case group comprised 60 patients with a history of ACS, while the control group consisted of 30 patients without a history of cardiovascular complaints. MTHFR A12980C gene polymorphism examination was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR RFLP) method at the Tropical Disease Center UNAIR Laboratory. RESULTS: Among the ACS group, 29 (48.1%), 13 (21.7%), and 18 (30%) of the individuals had AA, AC, and CC genotype patterns, respectively. In the control group, 16 individuals had AA (53.3%), 6 AC (20%), and 8 CC (26.7%). The C allele variant was identified in 41% of the ACS group and 37% of the control group. The odds ratio (OR) for the incidence of ACS was 1.195 (95% confidence interval [CI]; 0.381-3.752), 1.241 (95% CI; 0.481-3.486), and 1.222 (95% CI; 0.381-3.752). Chi-square analysis revealed no association between MTHFR A1298C gene polymorphism and the incidence of ACS (P > 0.05). CONCLUSIONS: MTHFR A1298C gene polymorphism did not significantly affect ACS incidence.

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